Abstract

Background

The predominant mechanism by which human tumors maintain telomere length is via telomerase.
In ~10% of tumor samples, however, telomere length is conserved, despite no detectable
telomerase activity, in part through activation of the alternative lengthening of
telomeres (ALT) pathway.

Methods

Results

We identified the presence of ECTR in primary leukemia cells from some of these samples,
which indicates the possible involvement of an ALT mechanism. Moreover, we found that
some samples exhibited both circular ECTR and telomerase activities, suggesting that
both mechanisms can contribute to the onset of CML.

Conclusion

We propose that ALT or the combined activities of ALT and telomerase might be required
for the early stages of leukemogenesis. These findings shed new light into the oncogenic
pathways responsible for the maintenance of telomere length in leukemia, which will
ultimately determine the effectiveness of anti-telomerase-based treatment protocols.